Normal Lab Values

Week 13: Cardiovascular System

Suggested readings from
Robbins 8th ed.
Congenital and Inflammatory Heart Diseases: pp.537-545 and 561-587
 
Ischemia and Cardiovascular Intervention: pp. 525-527, 529-537, and 545-561

Pathology Cases for Week 13

Review Items for Week 13

 

Pathology Case Descriptions

CASE NUMBER 25
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Clinical History: A 9-year-old female had two previous attacks of rheumatic fever. She entered the hospital for the third time with painful swollen joints, fever, and pulmonary edema. She died with signs of progressive heart failure.

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(Summary of Gross Findings - click here)
Her heart weighed 380 grams (normal for this age is about 115 grams). The pericardium was covered with a fibrinous exudate. The left ventricle was dilated and the myocardium was flabby. The mitral valve was slightly thickened as were the chordae tendinae. There was a MacCallum's patch in the left atrium. The liver weighed 780 grams (normal 750 grams). There was centrilobular congestion ("nutmeg liver").
(Summary of Microscopic Findings - click here)
The section includes the entire thickness of the myocardium and is taken through the mitral valve so that both left atrial and left ventricular myocardium are present in the section. The epicardium shows a prominent layer of fibrin on the surface; deep to this is young connective tissue with many capillaries, fibroblasts, and chronic inflammatory cells, i.e. granulation tissue. Thus, this is an organizing fibrinous pericarditis. There is also myocarditis present. The myocardial inflammation includes Aschoff bodies of different ages. Identify very early, intermediate and healed foci. The presence of Aschoff bodies indicates that this is a rheumatic myocarditis. Note also marked endocardial thickening due to inflammation and scarring, especially in the left atrium (MacCallum's patch).
(Review Normal Histology - click here)
Norm No. 13 Heart
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Normal heart tissue sections demonstrate no evidence of fibrosis or hemorrhage.  Cardiac myocytes have moderately sized centrally located nuclei. Normal myocytes are not brightly eosinphilic. Normally no inflammation is seen.  Normal cardiac myocytes do not show hypertrophy.

 

25-1. This patient had:

  1. Rheumatic endocarditis
  2. Rheumatic myocarditis
  3. Rheumatic pericarditis
  4. ALL of the above

ANSWER

 

25-2. These slides illustrate prominent owl-eye macrophages that are deemed pathognomonic for this disease called:

  1. Aschoff cells
  2. Anitschkow cells
  3. MacCallum cells
  4. Libman-Sacks cells

ANSWER

 

25-3. The multinucleated macrophages are termed:

  1. Aschoff cells
  2. Anitschkow cells
  3. MacCallum cells
  4. Libman-Sacks cells

ANSWER

 

 

 

CASE NUMBER 195 (micro case 4)
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Clinical History: A 67-year-old male had rheumatic heart disease for thirty years. Three months prior to death he began to have episodes of fever and chills accompanied by signs of worsening congestive heart failure. Splinter hemorrhages and purpuric skin rashes were noted three weeks before death.

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(Summary of Gross & Lab Findings - click here)
Splinter hemorrhages were observed at digit tips. Blood cultures grew alpha-hemolytic streptococci. The alpha hemolysis on blood agar typical of Streptococcus viridans is shown. Gram stain shows gram positive cocci in chains.The heart weighed 400 grams. There was thickening of the mitral valve leaflets and the chordae tendineae. Many friable calcified pink-gray granular verrucae were present on the valve. In addition, a large vegetation of the same type was found on the left auricular endocardium.
(Summary of Microscopic Findings - click here)
The section represents a portion of mitral valve, left atrium and left ventricle. The valve is greatly thickened and damaged. It is infiltrated with acute and chronic inflammatory cells, and shows a zone of necrosis and fibrosis in the central portion of the valve. The myocardium shows slight focal fibrosis, and focal acute inflammatory infiltration in some sections.
(Review Normal Histology - click here)
Norm No. 13 Heart
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Normal heart tissue sections demonstrate no evidence of fibrosis or hemorrhage.  Cardiac myocytes have moderately sized centrally located nuclei. Normal myocytes are not brightly eosinphilic. Normally no inflammation is seen.  Normal cardiac myocytes do not show hypertrophy.

 

195-1. MOST cases that present with these findings are caused by:

  1. Chlamydiae
  2. Rickettsiae
  3. Fungi
  4. Bacteria

ANSWER

 

195-2. In this particular patient the MOST LIKELY causative organism was:

  1. Group A Streptococci
  2. Viridans Streptococci
  3. Staphylococcus aureus
  4. Staphylococcus epidermidis

ANSWER

 

195-3. The organism MOST LIKELY to infect normal heart valves is:

  1. Group A Streptococci
  2. Group B Streptococci
  3. Viridans Streptococci
  4. Staphylococcus aureus

ANSWER

 

195-4. The organism MOST OFTEN associated with prosthetic valve endocarditis is:

  1. Group B Streptococci
  2. Viridans Streptococci
  3. Staphylococcus aureus
  4. Staphylococcus epidermidis

ANSWER

 

195-5. The organism MOST OFTEN associated with infective endocarditis in IV drug abusers is:

  1. Group B Streptococci
  2. Viridans Streptococci
  3. Staphylococcus aureus
  4. Staphylococcus epidermidis

ANSWER

 

195-6. The heart valve MOST OFTEN affected by infective endocarditis in IV drug abusers is the:

  1. Aortic valve
  2. Mitral valve
  3. Pulmonic valve
  4. Tricuspid valve

ANSWER

 

 

CASE NUMBER 31
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Clinical History: This 45-year-old man had been well until he was awakened by chest pain that radiated to both arms and neck and was associated with diaphoresis. His blood pressure was 160/110. He was treated with diuretics (Lasix), but he continued to gain weight. He developed a friction rub. Two days after the onset of the chest pain he had a cardiac arrest and died.

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(Summary of Gross Findings - click here)
The heart was slightly enlarged weighing 460g. There was severe atherosclerosis of all the major coronary arteries with a recent thrombotic occlusion of the proximal left anterior descending coronary artery. A recent transmural infarct was present in the left ventricle that involved the interventricular septum and the papillary muscle.
(Summary of Microscopic Findings - click here)
The slide includes a transmural section of the left ventricle. Nearly the entire section is involved by infarct. However, there is a thin rim (5 to 10 cell layers) of endocardial myocytes which have survived because of diffusion of oxygen and nutrients from the ventricular cavity. Other viable myocytes can be found around larger blood vessels within the section. The intense hypereosinophilia of the necrotic myocytes can best be appreciated by comparing the thin rim of lighter staining subendocardial myocytes with the deeper cells. Note also the karyolysis that is characteristic of coagulation necrosis. In some areas there is little inflammatory response. This observation is explained by microvascular necrosis which does not allow access of circulating leukocytes to these areas. In other areas, especially in the epicardial half of the infarct, there is an intense acute inflammatory response. Many intact neutrophils can be seen. In addition, there are many nuclear fragments from lysed neutrophils. Macrophage activity is not evident. These features of the inflammatory response indicate that the infarct was approximately three to four days old. Note also that the inflammation extends to the epicardial surface and that there are deposits of fibrin on the epicardium. This is called fibrinous pericarditis. The granular grey material seen within some blood vessels is barium sulfate, which was injected to permit post-mortem study of the coronaries by radiography.
(Review Normal Histology - click here)
Norm No. 13 Heart
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Normal heart tissue sections demonstrate no evidence of fibrosis or hemorrhage.  Cardiac myocytes have moderately sized centrally located nuclei. Normal myocytes are not brightly eosinphilic. Normally no inflammation is seen.  Normal cardiac myocytes do not show hypertrophy.

 

What is the MOST LIKELY diagnosis?

ANSWER

 

31-1. The event MOSTLIKELY associated with this patient’s problem was:

  1. Occlusion of a coronary vein
  2. Occlusion of a coronary artery
  3. Stabbed with ice pick
  4. Broken heart

ANSWER

 

31-2. What microscopic feature BEST describes what happened to the nucleus?

  1. Pyknosis
  2. Karyorrhexis
  3. Karyolysis
  4. Apoptosis

ANSWER

 

31-3. What molecular events led to the increase eosin staining of the dead myocytes?

  1. Loss of ribosomes
  2. Protein denaturation
  3. Protein synthesis
  4. A & B

ANSWER

 

31-4. The event MOST LIKELY associated with this patient’s problem was:

  1. Fixed coronary obstruction
  2. Plaque disruption
  3. Occlusive thrombus
  4. Hypovolemic shock

ANSWER

 

31-5. What microscopic feature in this patient indicates that this infarct is at least 24 hours old?

  1. Coagulation necrosis & loss of nuclei
  2. Wavy fibers
  3. Macrophage infiltrate
  4. Granulation tissue

ANSWER

 

31-6. What microscopic feature is MOST INDICATIVE of reperfusion of ischemic myocardium with irreversible injury?

  1. Necrosis with contraction bands
  2. Endothelial swelling
  3. Wavy fibers
  4. Hypereosinophilic cytoplasm

ANSWER

 

31-7. What artery was MOST LIKELY occluded in this patient?

  1. Left circumflex coronary artery
  2. Left anterior descending coronary artery
  3. Right coronary artery
  4. Impossible to determine

ANSWER

 

31-8. What myocardium is the MOST VULNERABLE to ischemic injury in hypovolemic shock?

  1. Subepicardial, left ventricle
  2. Mid-myocardial, left ventricle
  3. Subendocardial, left ventricle
  4. Subendocardial, right ventricle

ANSWER

 

 

 

CASE NUMBER 286
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Clinical History: This 64-year-old male had two episodes of myocardial infarction followed by congestive heart failure during the eight months prior to death. Death was preceded by arrhythmia.

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(Summary of Gross Findings - click here)
The heart was markedly hypertrophied (740 grams) and dilated. There was marked coronary atherosclerosis with an old occlusion of the left anterior descending vessel. A healed infarct involved the anteroseptal and apical region of the left ventricle. A mural thrombus which is not shown here covered much of the infarct.
(Summary of Microscopic Findings - click here)
The slide includes a transmural section of the anterior free wall and anterior portion of the interventricular septum. There is a broad band of dense, highly collagenized scar tissue replacing the middle layer of myocardium; patchy scarring interspersed with hypertrophied cardiac myocytes is present on either side of this dense scar. The endocardium is markedly thickened and there is organizing mural thrombus between cardiac trabeculae and extending into the lumen. Some myocytes in the subendocardial layer show sarcoplasmic vacuolization, a chronic degenerative change termed "myocytolysis".
(Review Normal Histology - click here)
Norm No. 13 Heart
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Normal heart tissue sections demonstrate no evidence of fibrosis or hemorrhage.  Cardiac myocytes have moderately sized centrally located nuclei. Normal myocytes are not brightly eosinphilic. Normally no inflammation is seen.  Normal cardiac myocytes do not show hypertrophy.

 

286-1. What is the YOUNGEST age that this infarct can be, given its microscopic appearance?

  1. 3 days
  2. 3 weeks
  3. 3 months
  4. 3 years

ANSWER

 

286-2. The possible age of the infarct can be determined as above because:

  1. No dead myocytes remain
  2. What was once myocardium is now scar
  3. No inflammation remains
  4. ALL of the above

ANSWER

 

286-3. A transmural infarct with the age of this lesion might be complicated by:

  1. Rupture
  2. Diffuse neutrophil infiltrate
  3. Necrosis
  4. Aneurysm

ANSWER

 

286-4. This patient was at greatest risk for infarction in the distribution of the:

  1. Anterior cerebral artery
  2. Middle cerebral artery
  3. Posterior cerebral artery
  4. Basilar artery

ANSWER

 

CARDIOVASCULAR PATHOLOGY Review Items

Key Vocabulary Terms (click here to search any additional terms on Stedman's Online Medical Dictionary)

anastomosis marantic endocarditis
aneurysm mitral valve prolapse
angina pectoris myocardial infarct
arrhythmia myocarditis
Aschoff body necrosis
cardiac tamponade pericarditis
cardiogenic shock Prinzmetal angina
cardiomyopathy reperfusion injury
congestive heart failure rheumatic fever
contraction band rheumatic heart disease
cor pulmonale stenosis
dextrocardia  sudden cardiac death
diastole systole
ductus arteriosus tetralogy of Fallot
endocardial fibroelastosis transposition of great vessels
endocarditis truncus arteriosus
foramen ovale unstable angina
heart failure valvular insufficiency 
hemopericardium valvular regurgitatioin 
hypertension valvular stenosis 
ischemic heart disease vegetation
Libman-Sacks endocarditis  

LEARNING OBJECTIVES

Absolutely critical information you must know to practice medicine is in bold font.
Important information that will be needed for routine patient care is in regular font.
Information about less common diseases that you may encounter in clinical practice and that will probably appear on examinations is in italics

  1. List the most common forms of heart disease in the United States

  2. Contrast and compare the clinical and pathologic features of the following:
    • congestive heart failure
    • high-output heart failure
    • left-sided heart failure
    • right-sided heart failure
    • cor pulmonale

  3. Discuss cardiogenic shock in terms of:
    • etiologic factors
    • pathogenesis
    • morphology
    • stages
    • clinical manifestations

  4. Discuss congenital heart disease in terms of:
    • genetic and environmental factors
    • types which result in:
      • left-to-right vs. right-to-left shunts
      • cyanotic vs. acyanotic disease
    • types which come to medical attention in:
      • infancy
      • childhood
      • adulthood

  5. Compare and contrast clinical and pathologic features of congenital heart disease:
    • atrial septal defect (ASD)
    • ostium primum
    • ostium secundum
    • venticular septal defect (VSD)
    • tetralogy of Fallot
    • endocardial cushion defects
    • hypoplastic left heart syndrome
    • patent ductus arteriosus (PDA)
    • transposition of the great vessels
    • coarctation of the aorta
    • preductal
    • postductal
    • anomalous pulmonary venous return

  6. Compare and contrast clinical and pathologic features of the following
    • endocarditis
    • myocarditis
    • pericarditis
    • pericardial effusion
    • cardiac tamponade
    • pancarditis

  7. Compare and contrast the clinical and pathologic features of the following
    • acute rheumatic fever.
    • chronic rheumatic heart disease

  8. Compare and contrast the clinical and pathologic features of valvular heart disease
    • calcific aortic stenosis
    • aortic insufficiency
    • mitral stenosis/insufficiency
    • mitral valve prolapse
    • mitral annular calcification
    • tricuspid insufficiency
    • pulmonic insufficiency
    • infectious endocarditis

  9. List long term complications associated with prosthetic heart valves

  10. Compare and contrast the clinical and pathologic features of the following:
    • dilated (congestive) cardiomyopathy
    • hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic stenosis (IHSS)
    • restrictive cardiomyopathy
    • endomyocardial fibrosis
    • eosinophilic (Loeffler) endomyocarditis
    • endocardial fibroelatosis

  11. Discuss coronary artery disease, in terms of:
    • epidemiology
    • risk factors
    • etiologic factors
    • pathogenesis
    • complications

  12. Develop an understanding of acute coronary syndrome, relationship to plaque rupture and thrombosis, develop an understanding of the role of interventional cardiology and bypass surgery and why these treatments are used.

  13. Discuss myocardial infarct, in terms of:
    • etiologic factors
    • risk factors
    • pathogenesis
    • morphology
      • evolution of morphologic changes with time
      • correlation of morphologic distribution of infarct with site of coronary artery disease
    • clinical, laboratory, and electrocardiography findings that change with time after the event
    • complications, including expected timing after the event
    • prognosis, and common causes of death with increasing time after the event

  14. Discuss sudden cardiac death, in terms of:
    • causes
    • relationship to arrhythmias
    • cardiac morphology

  15. Discuss the following cardiac tumors
    • myxoma
    • rhabdomyoma
    • lipoma
    • metastatic

 

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